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Re: F1ash post# 158855

Sunday, 07/22/2018 8:44:46 AM

Sunday, July 22, 2018 8:44:46 AM

Post# of 517546
F1ash, thanks for the great effort and for this information. w/any luck this week could include the most important 3-5 days in many, many lives.

At least validation of the sigma1 approach if not A2-73 in particular.

“We therefore evaluated the effect of ANAVEX2-73 and PRE-084, a reference s1R agonist, on preservation of mitochondrial integrity in Aß25-35-injected mice. In isolated mitochondria from hippocampus preparations of Aß25-35 injected animals, we measured respiration rates, complex activities, lipid peroxidation, Bax/Bcl-2 ratios and cytochrome c release into the cytosol. Five days after Aß25-35 injection, mitochondrial respiration in mouse hippocampus was altered. ANAVEX2-73 (0.01-1 mg/kg IP) restored normal respiration and PRE-084 (0.5-1 mg/kg IP) increased respiration rates. Both compounds prevented Aß25-35-induced increases in lipid peroxidation levels, Bax/Bcl-2 ratio and cytochrome c release into the cytosol, all indicators of increased toxicity. ANAVEX2-73 and PRE-084 efficiently prevented the mitochondrial respiratory dysfunction and resulting oxidative stress and apoptosis. The s1R, targeted selectively or non-selectively, therefore appears as a valuable target for protection against mitochondrial damages in AD.”


https://bscb.org/learning-resources/softcell-e-learning/mitochondrion-much-more-than-an-energy-converter/

“Mitochondria: determinators
Recent research indicates that in addition to converting energy mitochondria play quite a large part in determining when a cell will die by ordinary cell death (necrosis) or programmed cell death (apoptosis). In apoptosis the mitochondrion releases a chemical, cytochrome c, and this can trigger programmed cell death (apoptosis).



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